Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3736_Библиотеки_им_академика_М_И_Перельмана
.pdf
104
https://t.me/medicina_free
Fig. 9.8 EKG of atypical atrial utter. The utter waves are less sawtooth in appearance, narrow, and organized as seen
in lead V1
L. Raines
Fig. 9.9 EKG of typical atrial utter. Note the negative utter waves in the inferior leads
• Reverse typical utter: utter waves are usu-
inverted in V1 [2, 3].
For some, differentiating atrial utter and
atrial tachycardia can be difcult. Some helpful
tips for ECG differentiation include the
following:
• Atrial rate: the atrial rate with atrial utter is
typically 250–350 bpm. Atrial rate with
atrial tachycardia is typically 150–250bpm
[2, 3].
• P wave morphology: in atrial utter the P
wave is usually inverted in leads II, III,
AVF.Atrial tachycardia usually shows upright
P wave in lead II, III, AVF [2, 3].
9 Atrial Arrhythmias
https://t.me/medicina_free
105
Management
Acute management of atrial utter is typically
focused on patient stability, anticoagulation for
stroke prevention, rate control, and conversion to
sinus rhythm. Atrial utter can be more difcult
to rate control than atrial brillation.
Acute Management
• In unstable patients in whom atrial utter is
poorly tolerated, direct current cardioversion
is a Class I recommendation [1].
• If a patient is stable and not in decompensated
heart failure or hypotensive, rate control with
AV nodal agents, such as the nondihydropyridine calcium channel blockers or beta blockers, can be attempted and have a class I
recommendation [1].
• IV amiodarone can be useful for rate control
in the absence of pre-excitation in patients
with utter and CHF when BB are contraindicated or ineffective (Class IIa) [1].
– Amiodarone has less negative inotropic
effect than BB/CCB and may produce less
hypotension [1].
– Though unlikely to convert a patient to
sinus rhythm, the potential to do so exists,
so potential risks and benets should be
considered for patients with utter ≥48 h
duration who are not adequately anticoagulated [1].
• In stable patients, conversion to sinus rhythm
can be achieved electrically with direct current cardioversion, or pharmacologically, with
an antiarrhythmic drug. Prior to proceeding
with cardioversion (either electric or pharmacologic), if arrhythmia onset is >48 h or
unknown, the presence of a left atrial appendage thrombus will need to be ruled out, either
by TEE or CT [1]. The most common antiarrhythmic agents (Chap. 7) used for converting
a patient to sinus rhythm include procainamide (1A antiarrhythmic), ecainide or
propafenone (1C antiarrhythmics), and amiodarone or Ibutilide (Class III antiarrhythmics).
Factors to consider when choosing an agent
for pharmacologic cardioversion include the
presence of structural heart disease, presence
of coronary artery disease, renal function, and
presence of ECG abnormalities such as IVCD/
bundle branch block, QRS duration, QT duration [2, 4]. In patients with a pacemaker or
debrillator with the presence of an atrial pacing wire, rapid atrial pacing is useful for acute
conversion of atrial utter (Class I)—this is
known as pace termination and recommendations for anticoagulation are the same as that
for pharmacologic and electrical cardioversion [1].
Anticoagulation
Anticoagulation should be considered in all
patients, especially if the onset of arrhythmia
duration is greater than 48 hours or unknown.
The CHA2DS2VASc score is used to calculate
stroke risk and components include CHF/LV dysfunction, hypertension, age, diabetes, prior
stroke/TIA, presence of vascular disease, and
gender. In the acute setting, if not contraindicated, IV heparin can be utilized with subsequent
transition to a direct oral anticoagulant (apixaban, rivaroxaban, or dabigatran) or warfarin
(once INR therapeutic). Anticoagulation should
be continued uninterrupted for at least 1month
post cardioversion, but possibly longer depending on the CHA2DS2VASC score [1, 5].
Ongoing Management
Long-term treatment for right-sided (typical and
reverse typical) atrial utter includes consideration of EP study and utter ablation (Class I recommendation) [1]. Because the re-entry circuit
involves the cavotricuspid isthmus, that area is
usually the target site for ablation. Ablation has a
very high success rate for treatment and elimination of right-sided atrial utter and should be
considered for most patients who are otherwise
not contraindicated for ablation. Patients will
need to be able to tolerate anticoagulation for up
to 1month prior to ablation and 4–6weeks post
utter ablation [1, 5].
For patients who are hemodynamically stable,
but otherwise contraindicated or do not wish to
undergo catheter ablation, beta blockers/calcium
106
https://t.me/medicina_free
L. Raines
channel blockers are useful with Class I recommendation [1].
As previously mentioned, patients with atrial
utter are at increased risk of developing or having concomitant atrial brillation. Up to 80% or
more of patients who undergo typical utter ablation will develop AF within 5years [1]. For this
reason, even if atrial utter is treated with ablation, ongoing surveillance for development of
atrial brillation should be considered, as well as
addressing risk factors. One method for ongoing
monitoring includes placement of an ambulatory
monitor to look for atrial brillation. Other methods emerging include wearables or patientcentered monitoring devices including watches
with ECG capabilities (e.g., Apple Watch®) and
the FDA-approved KardiaMobile® EKG
monitor.
Atrial Fibrillation
Atrial brillation is a relatively common arrhythmia and prevalence increases with age (Table9.1).
Symptoms associated with atrial brillation have
a wide distribution and range from completely
asymptomatic to severe. It is typically associated
with underlying structural heart disease (CAD,
CHF, valvular heart disease) and other chronic
Table 9.1 Denitions of atrial brillation
• Paroxysmal AF—self-terminating or intermittent;
resolves spontaneously or within 7days of onset [5]
• Persistent AF—rhythm is sustained greater than
7days. Fails to self-terminate but can be terminated
with pharmacologic or electric cardioversion [5]
• Long-standing persistent AF—continuous AF of
greater than 12months duration [5]
• Permanent AF—this term is used when the decision
has been made to stop attempts at restoring sinus
rhythm [5]
• Nonvalvular AF—AF that occurs in the absence of
moderate to severe mitral stenosis or a mechanical
heart valve [6]
• Valvular AF—generally refers to AF that occurs in
the setting of moderate to severe mitral stenosis or in
the presence of an articial (mechanical) heart valve
[6]
conditions, such as hypertension and diabetes [2,
5]. Atrial brillation is a progressive condition in
which episodes generally increase in frequency
and duration over time and may become persistent if left untreated. Similar to atrial utter, atrial
brillation is associated with increased risk of
stroke and CHF.
Anatomy andPhysiology
Atrial brillation is a supraventricular arrhythmia
that is characterized by uncoordinated atrial
activity, with atrial rates >350bpm [2, 4, 5]. As a
result, there is a decrease in the atrial mechanical
function with an associated irregular ventricular
response. The uncoordinated atrial activity results
in the loss of effective atrial contraction, also
known as “atrial kick”, and can decrease ventricular lling and cardiac output [4, 5]. The mechanisms that underlie AF are likely multifactorial
and involve multiple independent reentrant wavelets that exist within the atria, and are primarily
initiated by focal triggers that originate at or near
the pulmonary veins in the left atrium [2, 4, 5].
Structural and electrophysiologic abnormalities
can alter the properties of atrial tissue and allow
for abnormal impulse initiation or conduction.
Some precipitants include alcohol, drugs, caffeine, exercise, stress/emotion, sleep apnea, obesity, and hyperthyroidism [4, 5].
Physical Exam Correlation
Symptoms can be variable and range from no
symptoms to fatigue, shortness of breath, palpitations/cardiac awareness, weakness, dizziness,
lightheadedness, hypotension, heart failure, and
even syncope. Some patients who are initially
asymptomatic may develop heart failure symptoms if tachycardia-induced cardiomyopathy
occurs. Some patients present with TIA or stroke
symptoms. If associated with valvular heart disease, a murmur may be present on exam. Pulse
rate will be irregularly irregular.
9 Atrial Arrhythmias
https://t.me/medicina_free
107
Imaging
• ECG/telemetry monitoring:
– Characteristic ECG ndings include irreg-
ular R-R intervals, absence of discrete P
waves, and irregular atrial activity (which
may be ne or coarse) [2, 5] (see Fig.9.10).
– There are several types of wearable devices
available as well, that have ECG recording
capabilities. One such device is the Apple
Watch™. Another device is the KardiaMobile® device (or AliveCor® monitor).
• Transthoracic echocardiogram:
– All patients with AF should have an echo-
cardiogram performed. This is helpful in
determining LVEF, evaluation of the LA
and RA sizes, and determine if there is any
concomitant valve disease.
• Transesophageal echocardiogram:
– A transesophageal echo is more sensitive
for evaluating possible left atrial appendage (LAA) thrombus and should be performed in patients being considered for
either pharmacologic or electric cardioversion if duration of AF is > 48h or unknown
[5] (see Fig.9.11).
• Cardiac CT:
– A structural cardiac CT can also evaluate
the LAA for thrombus reliably.
• Ischemic evaluation in those without previ-
ously diagnosed CAD is helpful in guiding
pharmacotherapy since some antiarrhythmics
are contraindicated in patients with underlying CAD. Options for ischemic evaluation
include stress testing, CT of the coronaries,
cardiac MRI with stress, or cardiac catheterization. Decision on which type of test is pursued is typically guided by associated
symptoms, history, and if any possible contraindication to a particular test exists (ex. renal
dysfunction for CT/catheterization, etc.).
• Thyroid testing to evaluate for clinical or sub-
clinical hyperthyroidism.
Management
• Rate control (Chap. 7).
– Beta blockers.
Metoprolol.
Atenolol.
Carvedilol.
Fig. 9.10 EKG of atrial brillation with irregular R-R
intervals. No discernible P waves or PR interval conrms
the diagnosis of AF. Irregular R to R intervals can be
rhythms other than AF: NSR with PAC’s, wandering atrial
pacemaker, MAT are often misdiagnosed as AF
108
https://t.me/medicina_free
Fig. 9.11 Image of clot seen in left atrial appendage
Esmolol.
Propranolol.
– Calcium
channel blockers—nondihydropyridine.
• Diltiazem.
• Verapamil.
– Digoxin.
– Amiodarone can be used for rate control in
certain situations.
– A heart rate control strategy (resting HR
<80 bpm) is reasonable for symptomatic
patients. – ACC/AHA/HRS and AFFIRM
[5, 6].
– A lenient rate control strategy (resting HR
<110bpm) may be reasonable if a patient is
asymptomatic and LV function preserved.–
ACC/AHA/HRS and AFFIRM [5, 6].
– Permanent pacemaker implant followed by
AV nodal ablation can be one method for
rate control if the arrhythmia is refractory
to pharmacologic therapy. However, this
L. Raines
method is irreversible and results in pacemaker dependency, so is usually reserved
as a last option [5, 6].
• Rhythm control.
• There are multiple considerations when choosing an appropriate antiarrhythmic agent,
including presence/absence of CAD, left ventricular function, LV wall thickness, renal
function, liver function, ECG characteristics
such as QT interval, presence of IVCD/BBB,
AV block, and other medications that can be
relative or absolute contraindications if used
alongside a particular antiarrhythmic [5, 6].
Drug selection is mainly guided by safety,
rather than efcacy [5]. Risks of initiating an
antiarrhythmic should be considered, including that of proarrhythmia. Antiarrhythmic
drugs can prolong the QT interval and risk
causing torsades de pointes [4–6]. We want to
avoid precipitating ventricular arrhythmias in
an attempt to suppress atrial arrhythmias.
• Antiarrhythmic drugs for the treatment of
atrial brillation (Chap. 7):
– Class IA [5, 6].
Disopyramide.
• Negative inotrope.
• May be desirable in patients with
hypertrophic cardiomyopathy associated with dynamic LVOT obstruction. Otherwise avoided in structural
heart disease.
• Strong anticholinergic side effects.
– Class IC—these agents are for use in
patients without CAD/CHF/structural heart
disease [5, 6].
Flecainide.
• Can be initiated as an outpatient.
• Monitor QRS duration: do not want
duration to exceed > 15% baseline.
Propafenone.
– Class III.
Amiodarone [2, 4–6].
• Can be initiated inpatient or
outpatient.
• Has a large volume of distribution
and long half-life, so typically loaded
at higher doses with subsequent
taper over several weeks.
9 Atrial Arrhythmias
https://t.me/medicina_free
109
• Probably the most effective antiarrhythmic for maintenance of sinus
rhythm for patients with AF.
• Can be used in patients with or without CHF or structural heart disease.
• Potential toxicities include liver, thyroid, lung, eye, skin among others
and need surveillance with LFTs/
TFTs every 6 months and yearly
PFTs/CXR and eye exams.
Dofetilide (Tikosyn®) [5, 7].
• Must be initiated in the inpatient setting with continuous telemetry and
serial ECG monitoring. Want QT prolongation no more than 15% baseline.
• Concern for QT prolongation and
torsades.
• MULTIPLE drug interactions and
contraindications.
• Dose adjusted based on QT interval,
renal function. Contraindicated if
baseline QT > 440 sec.
Dronedarone [5].
• A structural analogue of amiodarone, but without the iodine component of amiodarone. Lower
incidence of adverse events compared to amiodarone, but also not as
effective.
• For use in patients who do not have
CHF.
• Monitor LFTs.
• Used less frequently due to
contraindications.
Sotalol [5].
• Renally cleared, so caution/contraindication in patients with CKD.
• Typically initiated inpatient, but
some experts may consider outpatient initiation in certain patients
with close surveillance.
Can worsen CHF.
Options for rhythm control other than antiar-
rhythmic therapy include:
– Cardioversion.
– Atrial brillation ablation [2, 4–6].
AF is often triggered by ectopic focal
discharges, which most commonly arise
from the left atrial myocardial cells that
extend into the pulmonary veins. Because
of this, atrial brillation ablation involves
pulmonary vein isolation as the primary
target for ablation. However, triggers can
also arise from the posterior wall of the
left atrium, ligament of Marshall, SVC/
IVC, coronary sinus, and LA appendage,
so these areas can also be ablated.
Though somewhat newer over the past
few years, hybrid atrial brillation ablation is becoming more common. This
type of ablation involves both electrophysiology and cardiac surgery, and
patients undergo both catheter-based
endocardial ablation, as well as surgical
epicardial ablation.
Catheter ablation has been shown to be
an effective treatment for patients who
previously failed antiarrhythmic medications, however recent studies have
shown ablation to be an appropriate rst
line treatment without rst needing to
trial and/or fail antiarrhythmic therapy.
Therefore, early referral to electrophysiology should be considered, especially
in younger patients.
• Anticoagulation.
• Anticoagulation should be considered in all
patients, especially if the onset of arrhythmia
duration is greater than 48h or unknown [5].
The CHA2DS2VASc score is used to calculate stroke risk and components include: CHF/
LV dysfunction, hypertension, age, diabetes,
prior stroke/TIA, presence of vascular disease,
and gender [6]. According to the most recent
ACC/AHA/HRS guidelines (2019), for
patients with a CHA2DS2VASc score of 2 or
greater in men, and 3 or greater in women,
oral anticoagulants are recommended [6].
– IV heparin.
In the acute setting, if not contraindicated,
IV heparin can be utilized with subsequent transition to a direct oral anticoagulant (apixaban, rivaroxaban, or dabigatran)
or warfarin (once INR therapeutic).
– Apixaban (Eliquis®) [5, 6].
Direct Factor Xa Inhibitor.
110
https://t.me/medicina_free
L. Raines
Dose based on weight (60 kg), serum
creatinine (1.5 mg/dL), and age
(80years).
Doses: 5 mg BID; otherwise, 2.5 mg
BID if meets 2 of the above criteria.
Able to be used in patients with ESRD
on dialysis.
Notable trial: ARISTOTLE.
– Rivaroxaban (Xarelto®) [5, 6].
Direct Factor Xa Inhibitor.
Dose based on renal function due to predominant renal clearance.
Administered once daily with the evening meal to ensure adequate
absorption.
Doses: 20mg daily; 15mg daily for creatinine clearance 30–49mL/min.
Notable trial: ROCKET AF.
– Dabigatran (Pradaxa) [5, 6].
Direct thrombin inhibitor.
Renally cleared, dose based on renal
function.
Doses: 150mg BID; 75mg BID for creatinine clearance 15–30mL/min.
Notable trial: RE-LY.
– Edoxaban [6].
Doses: 60mg daily for creatinine clearance 50–95 mL/min; 30 mg daily for
creatinine clearance 15–50mL/min.
Direct Factor Xa inhibitor.
Notable trial: ENGAGE-AF.
– Warfarin [5, 6].
A vitamin K antagonist with multiple
action sites along the coagulation
cascade.
Requires regular PT/INR monitoring
with goal 2–3 for AF in the absence of a
mechanical heart valve.
Warfarin is the recommended oral anticoagulant for those with mechanical
heart valves and target INR is based on
the type and location of the prosthetic
valve. (Supported by results from the
RE-ALIGN trial).
Bridging is required for patients with
AF and a mechanical heart valve if the
procedure requires warfarin interrup-
Notable points regarding the newer direct oral anticoagulants (DOACs). More information can be found by referencing the trials noted above, as well as specic drug
packaging inserts
Fewer drug interactions than warfarin
More rapid onset/offset
Less risk of intracranial bleeding when compared with
warfarin
Bridging with heparin should be individualized and
may not be needed
DOACs are not to be utilized in patients with valvular
AF or mechanical valve prosthesis.
Twice daily dosing (apixaban, dabigatran) vs daily
dosing (rivaroxaban, edoxaban)
Rivaroxaban should be taken with food
Consideration and dose adjustment in patients with
CKD and ESRD
tion. For patients with AF and without a
mechanical heart valve, decisions on
bridging should balance risk of stroke
and risk of bleeding, as well as the duration of time off anticoagulation.
Reversal agent: vitamin K.
Left Atrial Appendage Occlusion
For patients with contraindication to long-term
anticoagulation, exclusion of the left atrial
appendage via a percutaneous strategy can be
considered [5, 6]. One such device for left
atrial appendage occlusion is the Watchman®
device. Another device is the Amplatzer
Amulet®. These devices are typically placed in
the cardiac catheterization lab or EP lab via a
femoral catheter approach. Patients will require
short-term anticoagulation after device placement but will not require long-term
anticoagulation.
Cryptogenic Stroke
If a person has a stroke with unknown cause or
etiology, and if external ambulatory monitoring
is unrevealing, placement of an implantable loop
recorder is reasonable to identify silent atrial
brillation.
Clinical Pearls
• DOACs have quicker onset, fewer drug interactions and lower bleeding risk than Warfarin.
9 Atrial Arrhythmias
https://t.me/medicina_free
111
• Warfarin is the drug of choice for valvular
atrial brillation.
• First-line treatment of SVT is always dependent on patient stability.
• Short RP tachycardias: typical AVNRT, orthodromic AVRT, junctional tachycardia.
• Long RP tachycardias: atypical AVNRT, atrial
tachycardia, sinus tachycardia.
• Avoid AV nodal blocking agents with WPW
(or pre-excited atrial brillation).
• Typical utter is counterclockwise, around the
CTI, with negative appearance of the utter
wave.
• The earlier, the better for atrial brillation
ablation.
References
1. Page RL, Joglar JA, Caldwell MA, Calkins H, Conti
JB, Deal BJ, Estes NAM 3rd, Field ME, Goldberger
ZD, Hammill SC, Indik JH, Lindsay BD, Olshansky
B, Russo AM, Shen WK, Tracy CM, Al-Khatib SM.
2015 ACC/AHA/HRS guideline for the Management
of Adult Patients with supraventricular tachycardia. J
Am Coll Cardiol. 2016;67(13):e27–e115.
2. Baltazar RF.Basic and bedside electrocardiography.
Philadelphia: Wolters Kluwer; 2009.
3. Wagner GS. Marriott’s practical electrocardiography. 10th ed. Philadelphia: Lippincott, Williams &
Wilkins; 2001.
4. Mann DL, Zipes DP, Libby P, Bonow RO, Braunwald
E, editors. Braunwald’s heart disease. A textbook of
cardiovascular medicine, vol. 1. 10th ed. Philadelphia,
PA: Elsevier; 2015.
5. January CT, Wann LS, Alpert JS, Calkins H,
Cigarroa JE, Cleveland JC Jr, Conti JB, Ellinor PT,
Ezekowitz MD, Field ME, Murray KT, Sacco RL,
Stevenson WG, Tchou PJ, Tracy CM, Yancy CW,
American College of Cardiology/American Heart
Association Task Force on Practice Guidelines. 2014
AHA/ACC/HRS guideline for the management of
patients with atrial brillation. J Am Coll Cardiol.
2014;64(21):e1–76.
6. January CT, Wann LS, Calkins H, Chen LY, Cigarroa
JE, Cleveland JC Jr, Ellinor PT, Ezekowitz MD, Field
ME, Furie KL, Heidenreich PA, Murray KT, Shea JB,
Tracy CM, Yancy CW. 2019 AHA/ACC/HRS focused
update of the 2014 AHA/ACC/HRS guideline for the
management of patients with atrial brillation. J Am
Coll Cardiol. 2019;74(1):104–32.
7. Tikosyn treatment guidelines.
Ventricular Tachycardia
https://t.me/medicina_free
RobertHipp
10
Introduction
Ventricular tachycardia (VT) is wide complex
tachyarrhythmia with a QRS duration greater
than 120ms and a heart rate greater than 100bpm
[1]. It is dened as 3 or more premature ventricular contractions with a heart rate greater than
120% of the underlying rate. It can be nonsustained (greater than 3 beats) or sustained (greater
than 30seconds or with hemodynamic compromise). In acute presentations, any wide-complex
tachycardia should be treated as VT until proven
otherwise.
VT can be described based on QRS morphology to include monomorphic, polymorphic, and
ventricular brillation. Monomorphic VT has a
consistent QRS morphology from beat to beat
[2]. Polymorphic VT has a consistent deviation in
QRS morphology between beats [2]. Ventricular
brillation (VF) is a disorganized tachyarrhythmia with no clear QRS complexes and leads to
sudden hemodynamic compromise given failure
of relevant cardiac contraction.
In some cases, VT is caused by the presence of
chronic ventricular scar which leads to abnormal
impulse formation and propagation. These presentations often have regular R-R intervals and
monomorphic morphology. VT can also occur
R. Hipp (*)
Cardiac Electrophysiology, Hospital of the University
of Pennsylvania, Philadelphia, PA, USA
e-mail: Robert.Hipp@pennmedicine.upenn.edu
acutely in the presence of ischemia. Arrhythmias
secondary to acute ischemia are often faster and
more irregular than ones caused by chronic scar
or structural heart disease.
Pathophysiology
The mechanism for initiation of VT is either
abnormal automaticity, triggered activity, or reentry. In the case of re-entry, there must be an
early stimulus such as a PVC as well as a substrate to sustain the arrythmia. Re-entry is the
most common mechanism of ventricular arrhythmias and often occurs in the presence of structural heart disease [3]. Triggered and automatic
ventricular arrythmias are less common and are
caused by changes to the cardiac action potential
resulting in abnormal impulse formation [1].
Re-entry
Ventricular Tachycardia is most caused by a reentrant circuit in the ventricle due to a direct
insult (such as an MI) leading to remodeling (scar
formation) [3]. Re-entrant circuits often cause
monomorphic VT with regular R-R intervals.
Scar- related re-entry is commonly seen in
patients with heart disease from infarction and
brosis, but can also occur with other types of
cardiomyopathies. Other causative conditions
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
R. Musialowski, K. Allshouse (eds.), Cardiovascular Manual for the Advanced Practice Provider,
https://doi.org/10.1007/978-3-031-35819-7_10
113
114
https://t.me/medicina_free
R. Hipp
include cardiac sarcoidosis, arrhythmogenic right
ventricular cardiomyopathy (ARVC), surgical
correction of congenital heart disease, and myocarditis [2].
Re-entry circuits form in the area or zone
between myocardial scar and healthy tissue.
Circuits can be subendocardial, epicardial, or
extend through the entire thickness of the myocardium [3]. These regions blending live myocytes with brotic areas allow for abnormal
impulse propagation and areas of slow conduction. When an appropriately timed premature
ventricular beat occurs, re-entry is triggered. A
single large scar can have several VT circuits
(with different QRS morphologies) arising from
it using different exit sites.
Automaticity
Abnormal automaticity leading to ventricular
arrhythmia is caused by changes in phase 4 of the
cardiac action potential where the myocardial
cells are spontaneously depolarizing at a considerably faster rate than normal [4]. Abnormal
automaticity is associated with acute, reversible
conditions such as electrolyte abnormalities,
hypoxemia, and acute MI [3].Some VT may not
be associated with underlying heart disease and
has characteristic locations and EKG appearance
(i.e., RVOT-VT).
Triggered Activity
QT prolongation occurs with lengthening of
the action potential duration (phase 3) and allows
for PVC to fall on the T wave, initiating polymorphic VT.Hypokalemia and a prolonged QT interval (either genetic Long QT syndrome or taking
QT offending medications) can increase the possibility of this arrhythmia [1]. Ion channel dysfunction (inherited or otherwise) may also
lengthen repolarization leading to the development of early after depolarizations (EADs) and
triggered extrasystoles [3].
Catecholaminergic polymorphic ventricular
tachycardia (CPVT) is a VT occurring with
increased catecholamine release (such as with
exertion) or during a severe emotional disturbance. This occurs in the setting of a structurally
normal heart without the brotic changes associated with reentry [3]. Bidirectional VT is a hallmark of CPVT but may also be seen with digoxin
toxicity.
Symptoms
Most patients are highly symptomatic when
experiencing ventricular tachycardias. Common
symptoms include dizziness, lightheadedness,
palpitations, or shortness of breath. In some
cases, particularly in the setting of fast VTs, the
patient can become hemodynamically unstable
and develop syncope or have a cardiac arrest.
Rarely, patients may have minimal symptoms
besides a generalized feeling of fatigue, especially if the VT has a slow rate.
Electrolyte imbalance, sympathomimetic drugs,
catecholaminergic polymorphic ventricular
tachycardia (CPVT), pause dependence, and QT
offending medications are also causes of VT
independent of scar or brotic changes [3]. Low
potassium, magnesium, and calcium levels are all
known to change action potentials, while congenital or medication acquired QT prolongation
impacts repolarization allowing for the development of VT, or more commonly torsade de
pointes.
Physical Exam
The patient in VT will have a tachycardic rate
with potential jugular venous pulsation “cannon
A waves” due to A-V dissociation. These waves
are caused by atrial contraction against a closed
tricuspid valve during the ventricular arrhythmia.
Blood pressure may be low, and patients may be
tachypneic. There may also be signs of compromised cardiac output including poor peripheral
Соседние файлы в папке Библиотека им академика М.И. Перельмана